Bauer S, Jakobs K H
FEBS Lett. 1986 Mar 17;198(1):43-6. doi: 10.1016/0014-5793(86)81181-4.
Treatment of intact human platelets and S49 lymphoma cyc- cells with the phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, impairs GTP-dependent and hormone-induced inhibition of adenylate cyclase, an action mediated by the inhibitory coupling protein Ni. In contrast, receptor-independent activation of Ni with subsequent adenylate cyclase inhibition induced by the stable GTP analog, guanosine 5'-[gamma-thio]triphosphate, was affected in neither the potency nor onset of Ni activation by the stable GTP analog, in both membrane systems studied. The data indicate that modification of Ni following phorbol ester treatment does not impair its activation by stable GTP analogs.
用佛波酯12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯处理完整的人血小板和S49淋巴瘤cyc - 细胞，会损害GTP依赖性以及激素诱导的腺苷酸环化酶抑制作用，这一作用由抑制性偶联蛋白Ni介导。相比之下，在研究的两种膜系统中，由稳定的GTP类似物鸟苷5'-[γ-硫代]三磷酸诱导的Ni的受体非依赖性激活以及随后的腺苷酸环化酶抑制，在稳定GTP类似物对Ni激活的效力和起始方面均未受到影响。数据表明，佛波酯处理后Ni的修饰并不损害其被稳定GTP类似物激活的能力。
